Display options
Cite
Qian LQ, Li XQ, Ye PH, et al. Downregulation of MACC1 inhibits the viability, invasion and migration and induces apoptosis in esophageal carcinoma cells through the phosphatase and tensin homolog/phosphoinositide 3-kinase/protein kinase B signaling pathway. Oncol Lett. 2017;14(4):4897-4905doi: 10.3892/ol.2017.6790.
Qian, L. Q., Li, X. Q., Ye, P. H., Su, H. Y., Wang, G., Liu, Y., Shen, G. H., & Gao, Q. G. (2017). Downregulation of MACC1 inhibits the viability, invasion and migration and induces apoptosis in esophageal carcinoma cells through the phosphatase and tensin homolog/phosphoinositide 3-kinase/protein kinase B signaling pathway. Oncology letters, 14(4), 4897-4905. https://doi.org/10.3892/ol.2017.6790
Qian, Li-Qiang, et al. "Downregulation of MACC1 inhibits the viability, invasion and migration and induces apoptosis in esophageal carcinoma cells through the phosphatase and tensin homolog/phosphoinositide 3-kinase/protein kinase B signaling pathway." Oncology letters vol. 14,4 (2017): 4897-4905. doi: https://doi.org/10.3892/ol.2017.6790
Qian LQ, Li XQ, Ye PH, Su HY, Wang G, Liu Y, Shen GH, Gao QG. Downregulation of MACC1 inhibits the viability, invasion and migration and induces apoptosis in esophageal carcinoma cells through the phosphatase and tensin homolog/phosphoinositide 3-kinase/protein kinase B signaling pathway. Oncol Lett. 2017 Oct;14(4):4897-4905. doi: 10.3892/ol.2017.6790. Epub 2017 Aug 23. PMID: 29085498; PMCID: PMC5649641.
Copy Download .nbib Format: NLM
Share it on

Oncol Lett. 2017 Oct;14(4):4897-4905. doi: 10.3892/ol.2017.6790. Epub 2017 Aug 23.

Downregulation of MACC1 inhibits the viability, invasion and migration and induces apoptosis in esophageal carcinoma cells through the phosphatase and tensin homolog/phosphoinositide 3-kinase/protein kinase B signaling pathway.

Oncology letters

Li-Qiang Qian, Xia-Qin Li, Peng-Hui Ye, Hao-Yuan Su, Gang Wang, Yan Liu, Gen-Hai Shen, Quan-Gen Gao

Affiliations

  1. Department of General Surgery, Wujiang No. 1 People's Hospital, Suzhou, Jiangsu 215200, P.R. China.
  2. Department of Gynaecology and Obstetrics, Health Center of Songling, Suzhou, Jiangsu 215200, P.R. China.

PMID: 29085498 PMCID: PMC5649641 DOI: 10.3892/ol.2017.6790

Abstract

As an oncogene, MACC1 serves an important function in cancer progression and metastasis. However, the effect of MACC1 in esophageal carcinoma (EC) remains to be fully understood. The present study assessed the association between MACC1 expression and the progression of EC cells. A small interfering (si)RNA was delivered into EC cells to downregulate MACC1 expression. The MTT assay demonstrated that EC cell viability was reduced by siRNA-MACC1. Decreasing MACC1 expression increased the apoptotic rate of EC cells compared with control cells. Transwell and Matrigel assays demonstrated that EC cell migration and invasion, respectively, were downregulated by siRNA-MACC1. Furthermore, knocking down MACC1 suppressed the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway by upregulating the expression of phosphatase and tensin homolog (PTEN), a tumor suppressor. The results of the present study revealed that MACC1 expression affected cellular functions of the EC cells through the PTEN/PI3K/Akt signaling pathway. Therefore, MACC1 may potentially serve as a novel biomarker and therapeutic target for EC.

Keywords: MACC1; esophageal carcinoma; phosphatase and tensin homolog; phosphoinositide 3-kinase; protein kinase B

References

  1. Cancer Epidemiol Biomarkers Prev. 2012 Jul;21(7):1126-34 - PubMed
  2. Cell. 2007 Jan 12;128(1):25-8 - PubMed
  3. World J Gastroenterol. 2004 Nov 15;10(22):3235-9 - PubMed
  4. Anticancer Res. 2011 Mar;31(3):777-80 - PubMed
  5. Oncotarget. 2016 Apr 5;7(14 ):18085-94 - PubMed
  6. Cell Physiol Biochem. 2015 ;35(3):983-96 - PubMed
  7. Tumour Biol. 2014 Mar;35(3):2537-48 - PubMed
  8. Arterioscler Thromb Vasc Biol. 2000 Apr;20(4):1006-12 - PubMed
  9. Anticancer Res. 2011 Apr;31(4):1141-5 - PubMed
  10. World J Gastroenterol. 2015 Jan 7;21(1):333-41 - PubMed
  11. PLoS One. 2012;7(9):e44764 - PubMed
  12. Nat Med. 2009 Jan;15(1):59-67 - PubMed
  13. Genet Mol Res. 2015 Dec 14;14(4):16819-26 - PubMed
  14. Int J Cancer. 2013 Sep 15;133(6):1419-30 - PubMed
  15. J Clin Oncol. 2006 May 10;24(14):2137-50 - PubMed
  16. N Engl J Med. 2003 Dec 4;349(23):2241-52 - PubMed
  17. PLoS One. 2013;8(4):e60821 - PubMed
  18. Pathol Oncol Res. 2013 Oct;19(4):749-53 - PubMed
  19. Cancer Res. 2010 Jul 1;70(13):5281-92 - PubMed
  20. J Cancer Res Clin Oncol. 2015 Aug;141(8):1353-61 - PubMed
  21. Anticancer Res. 2010 Sep;30(9):3441-4 - PubMed
  22. Cancer Lett. 2015 Feb 1;357(1):242-53 - PubMed
  23. Bull Cancer. 2009 Apr;96(4):379-89 - PubMed
  24. Ann Surg. 2013 Jun;257(6):1089-95 - PubMed
  25. Oncol Lett. 2012 Oct;4(4):783-791 - PubMed
  26. Int J Cancer. 1999 Dec 10;83(6):870-873 - PubMed
  27. Cell Biosci. 2013 Mar 18;3(1):16 - PubMed
  28. CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 - PubMed
  29. Hepatology. 2008 Dec;48(6):2047-63 - PubMed
  30. World J Gastroenterol. 2012 Jun 21;18(23):2995-3003 - PubMed
  31. Asian Pac J Cancer Prev. 2015;16(1):195-9 - PubMed
  32. Ann Surg. 2001 Jul;234(1):25-32 - PubMed

Publication Types